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Description

While the focus on understanding factors that contribute to adult malignancy has centered on adult exposures, there is evidence that in utero alterations in energy metabolism resulting in difference in fetal growth contribute to a wide variety of diseases including cancer. Both high and low birth weights in mice and humans have been linked to adulthood cancers such as breast, colorectal, and hematologic malignancies. Recently, the incidence and aggressiveness of prostate cancer in humans have also been associated with increased birthweight. In addition, rodent studies have demonstrated that changes in maternal bioenergetics by dietary alterations shortened latency to developing other endocrine related malignancies such as mammary tumors. Due to the fact that the prostate and the uterine endometrium are both hormone responsive and a glandular tissue similar to breast we speculated that prostate and endometrial cancer in mice may demonstrate the same predisposition based on maternal diet.
In the data to be presented, we investigate whether maternal high-fat diet (HFD) in mice affects incidence of prostate hyperplasia in offspring. Using three independent assays, we demonstrate that maternal HFD is sufficient to initiate prostate hyperproliferation in adult male offspring. HFD exposed prostate tissues do not increase in size, but instead concomitantly up-regulate apoptosis. Maternal HFD-induced phenotypes are focally present in young adult subjects and greatly exacerbated in aged subjects. HFD-exposed prostate tissues additionally exhibit increased levels of activated Akt and deactivated Pten. Taken together, we conclude that maternal HFD diet is a candidate modifiable risk factor for prostate cancer initiation in later life. We have a potential mechanism identified and we are also looking at the females for uterine endometrial hyperproliferation as well. Finally, mice with targeted deletions of the tumor suppressors, PTEN and p53, in prostate (probasin Cre) and uterus (PR cre) are used to see if maternal HFD decreases the latency time to develop cancer in these predisposed mice.

Objectives

Objectives

In the data to be presented, we investigate whether maternal high-fat diet (HFD) in mice affects incidence of prostate hyperplasia in offspring. Using three independent assays, we demonstrate that maternal HFD is sufficient to initiate prostate hyperproliferation in adult male offspring. HFD exposed prostate tissues do not increase in size, but instead concomitantly up-regulate apoptosis. Maternal HFD-induced phenotypes are focally present in young adult subjects and greatly exacerbated in aged

Kyle Malter earned a degree in Animal Science and a DVM degree from the University of Missouri. After graduation, Kyle worked in an equine and small animal clinic in North Carolina for one year before transferring to Iowa. He practiced in a small animal hospital in Des Moines for three years and then in a mixed-animal practice for two years.

Kyle joined Boehringer Ingelheim Vetmedica, Inc. in 2010 as a Technical Services Veterinarian. He was recently appointed to the role of Technical Manager for Metacam and pet vaccines in Veterinary Medical Affairs. While at BIVI Kyle studied at the University of Iowa and became board-certified in the American College of Veterinary Preventive Medicine. He expects to earn a Masters in Public Health degree in December 2015.

Current Accreditations

This course has been certified by or provided by the following Certified Organization/s: